Cardiovascular effects of small peptides of the renin angiotensin system
The renin‐angiotensin system (RAS) is a unique hormonal cascade which is composed by multiple enzymes and effector peptides. Recently, new peptides presenting biological activity have been discovered, increasing the complexity of the RAS. Here, we evaluated the effects of small peptides of the RAS i...
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Veröffentlicht in: | Physiological reports 2017-11, Vol.5 (22), p.n/a |
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Sprache: | eng |
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Zusammenfassung: | The renin‐angiotensin system (RAS) is a unique hormonal cascade which is composed by multiple enzymes and effector peptides. Recently, new peptides presenting biological activity have been discovered, increasing the complexity of the RAS. Here, we evaluated the effects of small peptides of the RAS in coronary bed of rats. Firstly, we examined the direct effect of small angiotensinergic peptides [Angiotensin (Ang) ‐(1–5), Ang‐(1–4) Ang‐(1–3), and Ang‐(1–2)] in coronary vessels. Noteworthy, it was observed that Ang‐(1–4), Ang‐(1–3), and Ang‐(1–2) caused a significant reduction in pressure perfusion. Because Ang‐(1–2) was the smallest peptide tested and presented the major effect, we decided to investigate its mechanisms of action. The effect of Ang‐(1–2) was partially dependent on the Mas receptor, nitric oxide release and angiotensin‐converting enzyme. Importantly, Ang‐(1–2) reduced the blood pressure of Wistar rats and SHR. Interestingly, SHR presented a more pronounced decrease in blood pressure levels than Wistar rats. Altogether, these data showed that angiotensinergic small peptides hold biological activities in coronary bed of rats.
A direct vasodilator effect of small peptides from the renin angiotensin system in coronary bed of rats has not been fully established, as well as, the mechanisms underlying this action. Our present results showed that small fragments derived from angiotensin peptides hold biological activities in coronary bed of rats. Among the peptides evaluated, Ang‐(1–2) presented the higher vasodilator effect, which was mediated by angiotensin‐converting enzyme, nitric oxide release and activation of Mas receptor. |
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ISSN: | 2051-817X |
DOI: | 10.14814/phy2.13505 |